Thirty years after the Center for Disease Control (CDC) reported the first US case of Acquired Immune Deficiency Syndrome (AIDS), the disease continues to stretch its shroud of death across the world. This, despite the billions of dollars that have been invested in the development of vaccines, spent on anti-retroviral therapies, and strewn about in condom distribution and sexual education schemes.

But there is a strange and disturbing trend now evident in the new cases of HIV/AIDS being reported, and it concerns women of reproductive age.

According to the most recent report of the Joint United Nations Programme on HIV/AIDS, published in 2009, close to 50% of all newly acquired Human Immunodeficiency Virus (HIV)-1 infections across the globe now occur in women of reproductive age. Only a decade before, in 1998, only roughly 36% of reported cases concerned women of all ages. Why this vast increase? Why, when treatment for HIV has become more accessible and the overall death toll has slowly been decreasing, are more and more women being infected? And why is the increase concentrated in women in their childbearing years?

Heterosexual intercourse is the point of transmission for the majority of these newly infected women. No surprise here. But sex is not just sex these days. Heavily funded population control programs have promoted, and even imposed, powerful, steroid-based contraceptive drugs on tens of millions of Third World women. What they trumpet as “greater global access to family planning methods” has in fact given the HIV virus greater access to women’s bodies by altering women’s local and systemic immunities, cervico-vaginal responses and protective vaginal flora—all in directions that make infection more likely.

Statistics gathered over the past 20 years reveal a parallel between an increase in contraceptive drug use and an increase in HIV-1 infections in women. Several epidemiological studies over the same period also seem to demonstrate a link. These studies were conducted with various cohorts of women from married mothers to single adolescents to “sex workers”, and were carried out, for the most part, among the populations of users of African family planning clinics. A link between the use of contraceptive drugs and HIV-1 disease acquisition and progression seemed evident, although most of the studies—for whatever reason—failed to draw any consistent or strong conclusions about this link. And none suggested that family planning programs ought to be modified or scaled back as a result.

One meta-analysis of 28 studies in 1999 suggested a positive association between oral contraceptives and HIV-1 incidence. A later study, however, carried out in 2006, claimed that there was no overall risk of acquiring HIV-1 as a result of such drug use. Such disparate results enable the promoters of population control programs to continue to rely on such contraceptive drugs, claiming, “the science is not settled.” Many of the organizations involved in such programs are, for obvious reasons, reluctant to offer clarity to women on the correlation between contraceptive use and HIV- disease prevalence in women. Indeed, several studies almost seem designed to deliberately obscure this fact.

Additional evidence of such a link comes from other studies that conclusively demonstrate that hormonal contraceptive use is positively associated with an increased risk of several other sexually transmitted infections (STI’s) such as Chlamydia.

So why are the studies involving HIV-1 transmission so inconclusive? Reasons include poor controls on variables such as age and sexual lifestyle variants, infrequent assessment, lack of follow-up and widely varying contraceptive delivery methods. Attempts at rendering comparative data are difficult, and some of the statistical compilations and some of the meta-analytical efforts, seemed designed to serve population politics.

There are other lacunae as well. Few studies consider the different effects of estrogen and progesterone—and their synthetic steroid-based counterparts–on vaginal and cervical structure and immunity. The studies that have been done broadly compare “hormonal contraceptive” use to HIV-1 acquisition and progression across a diverse range of deliverables–oral, injectible, intra-uteral, etc.—that are lumped together under one generic “hormonal contraceptive” title. The most common such amalgamation, Combined Oral Contraceptives (COC’s), consists of both hormonal (estrogen-like compounds) and steroidal (progestin) agents that work together to prevent ovulation, taken daily as “the pill.”

Other forms of contraceptive delivery include progestogen-only, such as the high-dose injectables Depo-Provera (DMPA) and Noristerat, moderate-dose pills, low-dose subdermal implants and laced intra-uterine devices (IUD’s). These steroidal forms of preventing pregnancy affect the female reproductive system somewhat differently than their estrogen-like counterparts. In low-dose delivery regimens, progestins cause a thickening of cervical mucus inhibiting sperm viability and penetration. In high-dose delivery, cervico-vaginal changes also occur: follicular development is halted along with ovulation and the endometrium is thinned. The progestogen-only effects are clear: they weigh heavily on women’s cervico-vaginal structure and protective flora, hence reducing a woman’s ability to ward off infection. As far back as 1991 abnormal changes in the condition of the cervix was found to be strongly been associated with increased susceptibility to HIV/AIDS acquisition.

The chain of reasoning is straightforward: Women who take drug-based hormonal and steroidal contraceptives are at increased risk of STI’s. HIV/AIDS is an STI. Therefore, women who take powerful steroid-based drugs called “hormonal contraceptives” are at increased risk of contracting the HIV virus.

It’s time that researchers and policy makers faced these facts responsibly, for women’s sake.

(Jennifer Kimball, Be.L., is the Executive Director of the Culture of Life Foundation.)